Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bursa- and thymus-dependent functions were examined in Marek's disease (MD)-susceptible normal chickens and in chickens treated with 5 and 16 mg of cyclophosphamide (CY) at the time of hatching. Chickens not exposed to Marek's disease virus (MDV) and treated with CY temporarily lost mitogenic response to concanavalin A but regained full response after 5 weeks. Bursa-dependent functions, such as presence of germinal centers in spleen and cecal tonsils, morphologic features of bursa, and sheep red blood cell antibody response were completely lost in chickens treated with 16 mg of CY and only partly retained in chickens treated with 5 mg of CY. In chickens exposed to MDV, the degree of thymus-dependent spleen cell mitogenic response was directly related to frequency and severity of MD. Chickens treated with 16 mg of CY had a mild mitogenic depression and low frequency and severity of MD lesions, whereas those treated with 5 mg of CY and those not treated had marked mitogenic depression and high frequency and severity of MD. Suppressions of bursa- and thymus-dependent functions by MDV alone were also evident when comparing MDV-exposed and nonexposed chickens. The results also indicate that presence of small, residual amounts of humoral factor(s) may enhance MDV oncogenesis.
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PMID:Cyclophosphamide-induced amelioration of Marek's disease in Marek's disease-susceptible chickens. 18 Aug 52

The effects of an altered content of dietary iodine and fat on the development of N-nitrosomethylurea-induced mammary tumors in rats were studied and correlated with thyroid and pituitary function studies. In three separate experiments, animals fed a semisynthetic diet containing 11.8% fat had an earlier time of tumor appearance and greater tumor burden than did controls maintained on a diet containing 4.6% fat. These diet-associated changes were markedly inhibited by ovariectomy, indicating that the tumor growth was hormone responsive. We examined the possibility that the diet with increased fat content enhanced tumor growth through alterations in prolactin metabolism but could find no consistent elevation in serum prolactin and no increase in pituitary prolactin synthesis in vitro. Our data further showed that rats on an iodine-deficient form of the high-fat diet had no greater tumor growth than did animals receiving an iodine-supplemented form of the same diet. We conclude from these results that iodine deficiency does not promote mammary tumorigenesis. An incidental finding of great interest was that ovariectomy led to a highly significant depression of thyroid-stimulating hormone production in vitro. This suggests that estrogens may directly influence thyroid-stimulating hormone synthesis in vivo and thus contribute to the sex-related differences in thyroid physiology.
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PMID:Effects of iodine deficiency and high-fat diet on N-nitrosomethylurea-induced mammary cancers in rats. 42 60

BALB/c mice infected with Rowson-Parr virus, a lymphatic leukemia virus isolated from the Friend complex, undergo a rapid depression of antibody response. Spleen cells from these mice in culture show a similar deficit in the response to stimulation with sheep red cells and inhibit the reactivity of normal splenocytes. In an attempt to reverse this immunosuppression, near normal responses were obtained in vitro from infected splenocytes by increasing antigen dose, by adding E. coli lipopolysaccharide, or, more effectively, by cocultivating with small numbers of unfractionated or T cell-depleted peritoneal exudate cells (PC), whereas other manipulations proved ineffective. PC did not prevent the inhibition of normal splenocytes by infected spleen cells, but exhibited substantial restorative activity in vivo. In similar experiments, the immunosuppression exerted by the entire Friend complex could be reversed by PC in vitro but not in vivo. These results indicate that a functional deficit of macrophages may be partially responsible for the immunological impairment induced by leukemia viruses and suggest rational approaches to evaluate the relevance of this impairment to oncogenesis.
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PMID:Reversal of immunosuppression induced by murine leukemia viruses. 107 70

Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol. Patient age does not appear, in itself, to be associated with more beta-blocker side effects. Side effects of the second category are rare. They include an unusual oculomucocutaneous reaction and the possibility of oncogenesis. There are also many drugs that interact with beta-blockers, which may increase toxicity. Finally, there are specific patient characteristics where one beta-blocker may be more effective and safer than another.
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PMID:Beta-adrenergic receptor blockers. Adverse effects and drug interactions. 289 72

The Epstein-Barr virus (EBV), a B lymphotropic virus, is involved in a growing number of immunopathological disorders benign or malignant. The X-linked lymphoproliferative syndrome and its multifaceted clinical expression in a unique situation described in this issue by Purtilo. Among recent findings, the association between EBV and idiopathic interstitial pneumopathy (also named cryptogenic fibrosing alveolitis), is to be noted (6). From a molecular biology view-point, in vitro immortalization of B lymphocytes by EBV is under a pluri-genic (EBNA 2, EBNA 1, LYDMA) control. The role of EBV in oncogenesis appears different in Burkitt's Lymphoma (BL) and in nasopharyngeal carcinoma (NPC). In development of African BL, EBV appears to initiate the multistage carcinogenic event, through an early and massive infection. Other events include specific depression of T-cell immunity by hyperendemic malaria and c-myc onc-gene activation through chromosome translocation. In the genesis of NPC, the role of EBV still remain to be clarified although the strong and consistent association between EBV and the undifferentiated carcinoma of the nasopharyngeal (NPC) around the world favours an etiological relationship. The simple detection of IgA antibodies to VCA and EA allows early detection of the NPC, thus permitting a 95% cure rate at 5 years post-radiotherapy. Such an early diagnostic is of paramount public health importance. Furthermore, IgA/VCA and IgA/EA antibodies characterize precancerous conditions, giving the theoretical possibility of preventive interventions.
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PMID:The Epstein-Barr virus (EBV): a Rosetta Stone for understanding the role of viruses in immunopathological disorders and in human carcinogenesis. 299 May 89

Although supported by a number of experimental models, the assumption assigning a crucial role to the immune system in the antineoplastic defense mechanisms has not been convincingly demonstrated so far for human tumors. Should the theory be correct, severe functional impairment of the immune system would obviously result in the occurrence of tumors with abnormally high frequency. Registry holdings systematically collecting pertinent information on the malignancies developed in patients with primary immunodeficiency diseases or in organ transplant recipients maintained on therapeutically-induced immune depression, as well as the observation of tumors occurring in patients treated with immunosuppressive agents and of second malignancies arising after radio- and/or chemotherapy of the primary tumor consistently indicate that depressed immunity is usually associated with an increased incidence of cancer as compared with that expected in the general control populations. However, not all types of tumors are increased to the same extent, in that lymphoreticular neoplasias (especially non-Hodgkin's lymphomas), acute leukemias as second tumors and, among solid neoplasms, squamous cell carcinomas are those most frequently reported. These observations suggest that even deeply impaired tumoricidal immune mechanisms may facilitate the growth of certain tumors only, especially of those arising from the cells of the immune system itself, in remarkable contrast with their frequency in the general population. Oncogenesis may be favoured in various states of depressed immunity by a number of ways. Their elucidation might have bearing on the comprehension of the more general phenomenon of the neoplastic transformation.
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PMID:[Immunological deficiency syndromes, immunosuppression by drugs and occurrence of neoplasms: a casual association?]. 409 54

Epidemiological data indicate that life style, including dietary "imbalances", play a major role in etiology of human cancers. Although two thirds of the world population suffer from varying grades of protein-caloric malnutrition (PCM) today, no consistent pattern is found to be associated wih PCM both in man and laboratory animals. At the tissue level, depression of cellular proliferation by prolongation of DNA-synthetic phase is a characteristic lesion of PCM. Due to changes in liver mixed function oxidases, metabolism of drugs is affected. The cell-mediated immunity is depressed and there is a defective mobilisation of macrophages. These alterations would modulate carcinogenesis; some tend to enhance, while others inhibit tumorigenesis. The balance of evidence suggest that PCM is unlikely to have dominant modulating influence on carcinogenesis.
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PMID:Implications of malnutrition in chemical carcinogenesis. 678 74

The Ah locus represents a complex "cluster" of genese controlling the induction of numerous drug-metabolizing enzyme "activities" by polycyclic aromatic compounds. Allelic differences at the Ah locus are reflected in the large differences in inducibility of cytochrome P1-450 and benzo[a]pyrene metabolism in numerous tissues when the mice receive the chemical daily in their diet. This experimental model system offers to the hematologist and clinical pharmacologist a means to study genetic differences in toxic chemical depression of the bone marrow, as well as a potential model to study aplastic anemia and leukemia explainable on a single-gene basis. The genetically "responsive" individual who is at increased risk for cancer caused by subcutaneous or topical or intratracheal polycyclic hydrocarbons is at decreased risk for toxicity of the bone marrow and leukemia caused by oral benzo[a]pyrene (when compared with the genetically "nonresponsive" individual receiving the same dose of the same xenobiotic). In other words, tissue sites in direct contact with the carcinogen develop cancer in responsive animals because of induced P1-450; tissues in distant sites of the body may develop malignancy in nonresponsive animals because more carcinogen reaches that tissue due to decreased P1-450 induction all over the body and therefore decreased detoxication. Not only the dct with the carcinogen develop cancer in responsive animals because of induced P1-450; tissues in distant sites of the body may develop malignancy in nonresponsive animals because more carcinogen reaches that tissue due to decreased P1-450 induction all over the body and therefore decreased detoxication. Not only the dct with the carcinogen develop cancer in responsive animals because of induced P1-450; tissues in distant sites of the body may develop malignancy in nonresponsive animals because more carcinogen reaches that tissue due to decreased P1-450 induction all over the body and therefore decreased detoxication. Not only the dose but the route of administration and the tissue in which the malignancy or toxicity develops are therefore very important in the interpretation of data from tumorigenesis or toxicity experiments involving P1-450 inducers such as polycyclic hydrocarbons. There exists sufficient evidence that heritable variation of the Ah locus occurs in man. Growing evidence indicates that persons with higher aryl hydrocarbon hydroxylase inducibility in their cultured mitogen-activated lymphocytes may have a statistically significantly increased risk for certain types of cancer and drug toxicity. It remains to be determined at the present time, however, whether this genotype can be used as a biochemical marker in the individual patient for predicting increased susceptibility to certain types of environmentally caused cancers or toxicity in man.
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PMID:Genetic differences in susceptibility to chemically induced myelotoxicity and leukemia. 701 19

While radiotherapy and antineoplastic chemotherapy often control malignancies they may, paradoxically, cause new cancers to develop as long-term complications. Although almost any type of neoplasm can occur, radiation-induced malignancies are most likely to affect the myelopoietic tissues and the thyroid gland. The former tissues are also most frequently involved by chemotherapy. The combination of intensive radiotherapy and intensive chemotherapy is particularly leukemogenic. Acute myeloid leukemia has occurred with increased frequency following treatment of Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma, ovarian cancer, polycythemia vera, carcinoma of the thyroid gland, and carcinoma of the breast. Radiation-induced malignancies usually occur in the field of irradiation. For example, radiotherapy for carcinoma of the cervix may be followed by the development of carcinomas of the endometrium, vagina, urinary bladder, colon , rectum, and anus, as well as mesotheliomas of the peritoneum and osteosarcomas of the pelvis. Tumors developing in an irradiated field include a substantial number of soft tissue sarcomas or osteosarcomas. There is a 20-fold increase of second cancers following treatment of childhood malignancies, mostly sarcomas of bone and soft tissues, but including leukemia, and carcinomas of the thyroid gland, skin, and breast. The latent period between radiotherapy and the appearance of a second cancer ranges from 2 years to several decades, often being 10-15 years. With chemotherapy the mean latent period is shorter, approximately 4 years. The mechanism of oncogenesis by radiotherapy or chemotherapy is poorly understood and probably involves a complex interplay of somatic mutation, co-oncogenic effects, depression of host immunity, stimulation of cellular proliferation, and genetic susceptibility. The danger of developing second malignancies following radiotherapy or chemotherapy emphasizes the need for lifelong follow-up of patients given these forms of treatment; particularly in those with a long life expectancy as are those treated for childhood neoplasms.
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PMID:Second neoplasms following radiotherapy or chemotherapy for cancer. 708 Nov 42

The 18th human chromosome is probably known mainly due to patients with Edwards syndrome, children dying usually during the first week of life, the syndrome being due to the presence of three chromosomes 18-trisomy. Some of its loci participate in oncogenesis either as cellular oncogenes (BCL2 in lymphomas), or antioncogenes (DCC--in colorectal carcinomas--Lynch I and Lynch II). It is assumed that some of the causes of maniac depression could be associated with chromosome no. 18.
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PMID:[The human genome--chromosome 18]. 748 75


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